Abstract EN:

The parabrachio-amygdaloid pathway, going from the parabrachial nucleus (PB) to the central nucleus of the amygdala (CeA), is implicated in the elaboration of physiological and emotional responses to noxious events. The PB also innervates the bed nucleus of the stria terminalis (BST) which, together with the CeA, constitute a broader morphofunctional macrostructure: the central extended amygdala (EAc). Our working hypothesis is that PB projections described separately toward the CeA, the BST and other EAc components might be part of a single PB-EAc pathway, aiming the entire EAc. Extracellular single-unit recordings were made in anesthetized rats revealing that a majority of CeA neurons respond to noxious stimulations, accurately encoding the intensity but not the localization of the stimulus. Orthodromic activity electrically evoked by PB stimulation suggests that at least part of the noxious information travels through the PB-CeA pathway. Anatomical characterization of this pathway using anterograde tract tracing techniques and axonal branching pattern reconstructions shows that PB neurones, generally peptidergic, send collaterals to more than one component of the EAc and innervate very few structures outside of it. Local knockout of the brain-derived neurotrophic factor (BDNF) gene in the PB leads to a loss of about one third of the analgesic properties of morphine without altering neither basal thresholds of noxious responses nor anxiety levels of animals. Since the BDNF produced in the PB is then forwarded to the CeA and to the BST, the consequences of this local knockout might implicate the PB-EAc pathway. Our results as a whole lead us to extend the parabrachio-amygdaloid projection to a PB-EAc pathway which would associate autonomic and noxious information and modulate pain perception according to the emotional state. Among the numerous neuropeptides found along the PB-EAc pathway, BDNF probably plays an important role in mediating adaptative mecanisms to pain.